Summary/Abstract. Massive efforts are underway to understand factors that contribute to the complex variation in late brain aging, ranging from optimally neurally healthy older adults to individuals afflicted by the devastating neurodegenerative changes resulting from Alzheimer?s disease (AD). At the forefront of brain aging research, The Human Connectome Project (HCP) Lifespan studies are currently in the process of acquiring an unprecedented dataset for understanding health, biological, and environmental and demographic factors that contribute to variation in neural development and brain aging and associated cognitive status. For the aging component of HCP-Lifespan, cutting edge neuroimaging data is being acquired in conjunction with heath, physiological, genetic, neuropsychological, and clinical scales in approximately 1200 individuals ranging in age from 36 years to 100+ across four data acquisition sites. Longitudinal data will be acquired on a subset of the sample allowing for descriptions of how brain structural and functional connectivity is altered with aging as well as complex modeling of a range of biological and demographic factors that differentially influence brain aging trajectories in the positive as well as negative directions. The HCP-Aging cohort includes individuals considered ?typically? aging and excludes individuals with any evidence of a range of systemic, neurological, and/or psychiatric disease processes that could be considered atypical in the population. Older individuals with overt cognitive impairment are excluded through telephone screening of cognitive status using the Modified Telephone Interview for Cognitive Status (TICS-M) and in person during study visit with the Montreal Cognitive Assessment (MoCA). Although these tests are valuable for excluding individuals clearly meeting criteria, the procedures are limited in sensitivity to detect early impairment, and would not be effective in detecting individuals with brain pathology that do not yet exhibit any impairment. Thus, it is likely that a portion of the older adults in the HCP-A cohort will be afflicted with Alzheimer?s disease (AD) neuropathology. This is particularly true given a focus on the HCP-Aging project to enroll individuals in the ?oldest-old? age category. We propose here to acquire positron emission tomography (PET) amyloid and tau data in a sample of individuals enrolled in the HCP-Aging study to map early stage AD pathology and to link AD pathology to brain connectivity data acquired in the HCP-Aging protocol. Data acquired in this project would ultimately be made publicly available and it is anticipated the work performed would lead to an expanded project to acquire AD biomarker data in a larger portion of the HCP-Aging cohort. Ultimately, these data could be used to understand early changes in brain connectivity in AD, develop prognostic imaging biomarkers, elucidate mechanisms of AD dementia, and to guide the development of possible novel therapies to target these early changes.